Cranial cruciate ligament injury in the dog: pathophysiology, diagnosis and treatment

Cranial cruciate ligament (CCL) disease in the dog is a multifactorial complex problem that requires a thorough understanding of the biomechanics of the stifle joint to be understood. Successful treatment of rupture of the CCL should be based on managing underlying anatomical and conformational abnormalities rather than attempting to eliminate the tibial cranial drawer sign. The cranial and caudal cruciate ligaments, the patella ligament and quadriceps mechanism, the medial and lateral collateral ligaments, the medial and lateral menisci and the joint capsule provide stability of the joint and load-sharing. The function of the stifle is also significantly influenced by the musculature of the pelvic limb. An active model of biomechanics of the stifle has been described that incorporates not only the ligamentous structures of the stifle but also the forces created by weight-bearing and the musculature of the pelvic limb. This model recognises a force called cranial tibial thrust, which occurs during weight-bearing, and causes compression of the femoral condyles against the tibial plateau. In middle-aged, large-breed dogs, forces acting on the CCL together with conformation-related mild hyperextension of the stifle and slightly increased tibial plateau slopes are suspected to cause progressive degeneration of the ligament. Palpation of craniolateral stifle laxity has become pathognomonic for CCL rupture; however, chronic periarticular fibrosis, a partial CCL rupture, and a tense patient, may make evaluation of instability of the stifle difficult. Surgical treatment is broadly separated into three groups: intracapsular, extracapsular, and tibial osteotomy techniques. Tibial osteotomy techniques do not serve to provide stability of the stifle but rather alter the geometry of the joint to eliminate cranial tibial thrust such that functional joint stability is achieved during weight-bearing. Visualisation of both menisci is a critical aspect of CCL surgery, irrespective of the technique being performed. Regardless of the surgical technique employed, approximately 85% of dogs show clinical improvement. However, many of these dogs will demonstrate intermittent pain or lameness. Post-operative management is an integral part of the treatment of CCL rupture, and significant benefits in limb function occur when formalised post-operative physiotherapy is performed.     

Caudal cruciate ligament damage in dogs with cranial cruciate ligament rupture

Objective: To investigate the incidence of caudal cruciate ligament (CaCL) damage in dogs with cranial cruciate ligament rupture (CCLR). Study Design: Prospective clinical study. Animals: Dogs (n=24) admitted for surgical stabilization of the stifle after CCLR and 8 healthy dogs with intact cranial cruciate ligament (CCL) and CaCL studied as controls. Methods: Preoperative radiographs and stifle joint images (arthrotomy, 6; arthroscopy, 18) were collected from dogs with CCLR. Severity of arthritis, synovitis, CCL damage, and CaCL damage were assessed using numerical rating scales. The CaCL was probed to determine whether minor fraying or a full thickness defect in the ligament was present. Data collected from the study population were compared with the control population of dogs. Results: The CaCL was damaged in 21/24 (88%) of dogs with CCLR; 6/24 (25%) had a full thickness defect in the CaCL. Severity of stifle synovitis and severity of damage to the CaCL were positively correlated (P<.05). Conclusions: The CaCL is damaged in a high percentage of dogs with CCLR. A significant and positive correlation exists between the degree of synovitis present and the extent of CaCL damage. Clinical Relevance: In dogs with CCLR, cruciate ligament pathology typically involves both the CCL and CaCL. As the severity of synovitis and the extent of CaCL damage are related, this observation supports the hypothesis that stifle synovitis may contribute to CCL and CaCL degeneration and subsequent damage.     

Localization of cathepsin K and tartrate-resistant acid phosphatase in synovium and cranial cruciate ligament in dogs with cruciate disease

OBJECTIVE: To localize cathepsin K and tartrate-resistant acid phosphatase (TRAP) in synovium and cranial cruciate ligament (CCL) of dogs with cruciate disease. ANIMALS: Dogs (n=15) with cruciate disease and ruptured CCL, and 12 dogs with intact CCL. METHODS: Synovium and CCL were examined histologically and cells containing cathepsin K or TRAP were identified immunohistochemically and histochemically, respectively. RESULTS: Increased cellular localization of cathepsin K and TRAP was detected in synovium and ruptured CCL in dogs with cruciate disease, when compared with tissues from dogs with intact CCL. Inflammation of synovium with TRAP+ macrophage-like cells was seen in 73% of dogs with CCL disease, but was not seen in dogs with intact CCL. The presence of cathepsin K and TRAP protein in synovium and CCL tissues was significantly correlated in dogs with CCL rupture. CONCLUSION: Inflammation of the epiligament of ruptured CCL with cathepsin K+ and TRAP+ macrophage-like cells forms part of a similar, more generalized chronic inflammatory change within the periarticular tissues of the stifle of a large proportion of dogs with CCL rupture. CLINICAL RELEVANCE: Production of matrix-degrading enzymes by the synovium may induce progressive pathologic rupture of the CCL. Therefore, these collagenolytic pathways may offer a novel target for medical therapy of joint inflammation in canine patients with cruciate disease.     

Risk factors for excessive tibial plateau angle in large-breed dogs with cranial cruciate ligament disease

OBJECTIVE: To identify risk factors for development of excessive tibial plateau angle (TPA) in large-breed dogs with cranial cruciate ligament disease (CCLD). DESIGN: Case-control study. ANIMALS: 58 dogs with excessive TPAs (ie, TPA >or= 35 degrees ; case dogs) and 58 dogs with normal TPAs (ie, TPA or= 35 degrees in both limbs were 13.6 times (95% confidence interval, 2.72 to 68.1) as likely to have been neutered before 6 months of age as were control dogs with TPA 相似文献   

The effect of cranial cruciate ligament insufficiency on caudal cruciate ligament morphology: An experimental study in dogs

OBJECTIVES: To investigate the effect of cranial cruciate ligament (CrCL) insufficiency on morphology of the canine caudal cruciate ligament (CdCL). STUDY DESIGN: In vivo experimental study. ANIMALS: Five adult foxhounds. METHODS: Two years after CrCL transection, the histologic appearance of CdCLs from CrCL-deficient and unoperated contralateral control (CrCL-intact) stifle joints were evaluated using light and transmission electron microscopy. RESULTS: CdCLs from CrCL-deficient joints had extracellular matrix changes, characterized by chondroid metaplasia and disruption of cell architecture. Percent of small-diameter fibrils in CdCLs from CrCL-deficient joints was significantly greater (P <.05) than that in CdCLs from CrCL-intact joints. Collagen fibril density in CdCLs from CrCL-deficient joints (41.09 +/- 5.39%) tended to be less than that in CdCLs from CrCL-intact joints (52.96 +/- 6.92%); however, this difference was not significant (P =.056). Mean eccentricity (ratio of minor to major diameters) of collagen fibrils was significantly (P <.0001) lower for CdCLs from CrCL-deficient joints (0.85 +/- 0.016) when compared with that for CdCLs from CrCL-intact joints (0.87 +/- 0.015). CONCLUSIONS: Significant alterations were found in the morphology of CdCLs from CrCL-deficient joints. These changes may be associated with repetitive microtrauma to the CdCL secondary to instability or enzymatic degradation in the hostile synovial environment of an unstable joint. CLINICAL RELEVANCE: Regardless of the cause, the switch to a predominantly small-diameter collagen fibril profile may reflect compromised material properties of the CdCL. This should be taken into account when considering surgical techniques that rely on the CdCL to stabilize CrCL-deficient stifles.     

Cranial cruciate ligament rupture in the dog—a retrospective study comparing surgical techniques

SUMMARY Three surgical techniques, grouped as intra-articular techniques, extra-capsular techniques and fibular head transposition, were used for repair of the cranial cruciate ligament (CCL)-deficient stifle in 113 dogs over a 4 year 4 month period. The clinical outcome of the techniques were compared using information provided by the owners and physical examination. Regardless of surgical technique, 85.7 to 91.0% of dogs showed clinical improvement after surgery. However, less than 50% of dogs became clinically sound on the operated leg and 9.0 to 14.3% of dogs remained persistently lame on the operated leg. No statistical association was found between result after surgery and age, body weight, sex, duration of injury before surgery, association with injury, tibial plateau angle, degree of radiographic osteoarthritis before surgery or the presence of concurrent medial meniscal injury. On physical examination, extra-capsular techniques appeared superior to the fibular head transposition in terms of joint stability and limb function. Concurrent medial meniscal injury necessitating meniscectomy existed in 48.0% of cases. Twenty-two percent of dogs ruptured their contralateral CCL at an average of 14 months after the first.     

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

The majority of studies on cranial cruciate ligament (CrCL) disease to date have been carried out on dogs that already sustained a CrCL rupture, which is the end-stage of the disease. Investigations have recently been carried out to study humoral and cellular immunopathological mechanisms in predisposed dogs before clinical rupture of the contralateral CrCL. The cruciate ligaments are mainly composed of collagen type I, and immune responses to collagen have been suggested as a cause of CrCL degradation in dogs. None of these investigations showed evidence that anticollagen type I antibodies alone initiate CrCL damage. However, in predisposed dogs a distinct anticollagen type I antibody gradient was found towards the contralateral stifle joint that eventually sustained a CrCL rupture, suggesting that there was an inflammatory process present in these joints before detectable joint instability occurred. The importance of cellular reactivity to collagen type I in cruciate disease also remains unclear. Peripheral blood mononuclear cell proliferation to collagen type I was very diverse in dogs with cruciate disease whereas some sham operated dogs and healthy dogs tested positive as well. It is not yet determined whether cellular reactivity to collagen type I exists locally in the stifle joints nor whether this could initiate CrCL degradation. Inflammatory processes within the stifle joint can alter the composition of the cruciate ligaments. In animal models of immune-mediated synovitis, the mechanical strength of the CrCL is significantly reduced. Immunohistochemical studies on synovial tissues from dogs with rheumatoid arthritis and dogs with cruciate disease revealed that the pathologic features are similar in both joint pathologies and that the differences are mainly quantitative. Joint inflammation induced by biochemical factors such as cytokines has been implied in CrCL degeneration. In several studies, the levels of pro-inflammatory and T helper cytokines were measured in dogs that sustained a CrCL rupture, but the exact role of the various cytokines in the pathogenesis of CrCL disease remains inconclusive. More recently, the levels of the cytokines have been investigated over time in predisposed dogs before and after CrCL rupture. IL-8 expression tended to be higher in stifle joints that will rupture their CrCL during the next 6 months than in those that will not, indicating an inflammatory process in these joints before clinical rupture. This review provides a comprehensive overview of all possible implications of humoral and cell-mediated immune responses published in dogs with cruciate disease together with publications from human joint diseases. Furthermore, this review highlights recent findings on cytokines and proteinases in the accompanying joint inflammation.     

Evaluation of ligament fibroblast viability in ruptured cranial cruciate ligament of dogs

OBJECTIVE: To determine fibroblast viability, assess development of apoptosis, and evaluate tissue hypoxia via histochemical, in-situ hybridization, or immunohistochemical staining in ruptured and intact cranial cruciate ligaments (CCLs) of dogs. ANIMALS: 32 dogs with ruptured CCLs, and 8 aged and 19 young dogs with intact CCLs. PROCEDURE: Markers of cell viability (lactate dehydrogenase [LDH]), apoptosis (terminal deoxynucleatidyl transferase-mediated deoxyuridine triphosphate-nick end labeling [TUNEL] method), and hypoxia (hypoxia-inducible factor-1alpha [HIF-1alpha] monoclonal antibody) were applied to CCL specimens; positive cells were assessed objectively (LDH) and subjectively (TUNEL and HIF-1alpha) in the main axial tissue component (core) and synovial intima and subintima (epiligamentous tissue). RESULTS: Viable fibroblasts were seen in all intact and ruptured CCLs. More nonviable cells were found in the core regions of ruptured CCLs and intact CCLs of young dogs than in the epiligamentous regions. Number of nonviable cells in the core region of ruptured CCLs was greater than that in intact CCLs of young and aged dogs, whereas the number in the epiligamentous region was similar in all specimens. The TUNEL and HIF-1alpha staining was only found in the epiligamentous region of ruptured CCLs. CONCLUSIONS AND CLINICAL RELEVANCE: Ruptured CCLs contained a high number of nonviable cells but not a great number of apoptotic cells. Repair processes in the epiligamentous region of the CCL include a metabolic response to hypoxia, suggesting that necrosis of ligament fibroblasts and transformation of surviving cells to a spheroid phenotype may be a response to hypoxia cause by microinjury or inadequate blood flow.     

Tibial osteotomies for cranial cruciate ligament insufficiency in dogs

Objective— To review the biomechanical considerations, experimental investigations, and clinical data pertaining to tibial osteotomy procedures for treatment of cranial cruciate ligament (CrCL) insufficiency in dogs.
Study Design— Literature review.
Methods— Literature search through Pub Med, Veterinary Information Network, Commonwealth Agricultural Bureau Abstracts, and conference proceedings abstracts (November 1977 to March 2007).
Results— Reported tibial osteotomy procedures attempt to eliminate sagittal instability (cranial tibial thrust) in CrCL-deficient stifles by altering the conformation of the proximal tibia. Functional stability can be achieved by decreasing the tibial plateau slope (cranial tibial closing wedge osteotomy [CTWO], tibial plateau leveling osteotomy [TPLO], combined TPLO and CTWO, proximal intraarticular osteotomy, chevron wedge osteotomy), altering the alignment of the patellar tendon (tibial tuberosity advancement), or both (triple tibial osteotomy). Clinical reports assessing the efficacy of these procedures frequently use subjective outcome measures, and the periods of follow-up evaluation are highly variable. Satisfactory results have been reported in most (>75%) dogs irrespective of the type of tibial osteotomy procedure.
Conclusions— Currently available data does not allow accurate comparisons between different tibial osteotomy procedures, or with traditional methods of stabilizing the CrCL-deficient stifle. Carefully designed long-term clinical studies and further biomechanical analyses are required to determine the optimal osteotomy technique, and whether these procedures are superior to other stabilization methods.
Clinical Relevance— Limb function in dogs with CrCL insufficiency can be improved using the currently described tibial osteotomy techniques.     

Partial rupture of the cranial cruciate ligament in dogs

Four cases of partial rupture of the craniomedial part of the cranial cruciate ligament (CCL) are presented. Clinical examination revealed only subtle signs of CCL injury. The cranial drawer sign was present in two dogs and in flexion only. As the cranial drawer sign is not always evident a tentative diagnosis of partial CCL rupture should be based on history, joint tenderness and joint effusion. Arthrotomy and careful probing of the ligament is indicated. In these cases the lesion was treated immediately after diagnosis to prevent further degeneration and possible total rupture of the ligament. A fascial graft using the ‘over the top’ reconstruction technique was performed leaving the intact portion of the ligament in situ. Follow-up examination after four to six months revealed normal limb function in three dogs whereas slight and periodic lameness persisted in one dog.     

Synovitis in dogs with stable stifle joints and incipient cranial cruciate ligament rupture: a cross-sectional study

Objective: To evaluate stifle joints of dogs for synovitis, before development of joint instability and cranial cruciate ligament rupture (CrCLR). Study Design: Cross‐sectional study. Animals: Dogs (n=16) with CrCLR and stable contralateral stifles; 10 control dogs with intact CrCL. Methods: Arthritis and tibial translation were graded radiographically. Synovitis severity and cruciate pathology were assessed arthroscopically. Presence of inflammatory cells in synovial membrane biopsies was scored histologically. CrCLR stifle pairs and control stifles were compared. Results: Radiographic evidence of arthritis, cranial tibial translation, and arthroscopic synovitis were increased in unstable stifles, when compared with stable contralateral stifles in CrCLR dogs (P<.05). Arthroscopic synovitis in both joints of CrCLR dogs was increased compared with controls, was correlated with radiographic arthritis (S_R=0.71, P<.05), and was present in all stable contralateral stifles. Arthroscopically, 75% of stable stifle joints had CrCL fiber disruption, which correlated with severity of synovitis (S_R=0.56, P<.05). Histologic evidence of synovitis was identified in all CrCLR dogs, but was only significantly correlated with arthroscopic observations in stable stifles (r²=0.57, P<.005). Conclusion: Synovitis is an early feature of the CrCLR arthropathy in dogs before development of joint instability clinically. Severity of synovitis is correlated with radiographic arthritis in joints with minimal to no clinically detectable CrCL damage.     

Long-term outcome of surgery for dogs with cranial cruciate ligament deficiency

Fifty-eight dogs with cranial cruciate ligament deficiency were assessed and treated surgically. At an average of 50 months postoperatively, the functional outcome was assessed by means of an owner-based clinical assessment and a clinical examination. Client-based data were available for 26 dogs and 20 dogs were reassessed after 50 months. The results were compared with the initial values and with data from an assessment 13 months postoperatively. The level of disability at 50 months was judged to be significantly less than initially. However, there were no differences between the initial assessments and those made after 50 months for the perceived 'effect of cold weather' and the dogs' 'ability to jump', despite both measures having improved after 13 months. Age and meniscal injury were identified as poor prognostic indicators for the long-term outcome. The equivalent joint on the contralateral limb deteriorated significantly during the study.     

Comparison of surgical treatment options for cranial cruciate ligament disease in large-breed dogs with excessive tibial plateau angle

Objective— To identify surgical techniques performed by veterinary surgeons for the treatment of cranial cruciate ligament disease in large-breed dogs with excessive tibial plateau angle (eTPA), compare their outcomes, identify risk factors for postoperative complications, and compare outcome and complication rate with tibial plateau leveling osteotomy (TPLO) in dogs without eTPA.
Study Design— Multicenter, case–control study.
Animals— eTPA group (TPA≥35°)=58 dogs (78 stifles); control group (TPA≤30°)=58 dogs (72 stifles).
Methods— Control and eTPA group dogs were identified. Medical records, radiographic reviews, and pet-owner interviews were used to identify surgical treatments performed, their complications, and outcome. Odds ratios with 95% confidence intervals, χ² tests, and t-tests were calculated to discern differences between eTPA and control-group dogs.
Results— TPLO was the most common treatment for eTPA. Owner-perceived outcome was superior for eTPA group dogs when TPLO resulted in TPA≤14° compared with those with postoperative TPA>14°. Loss of tibial plateau leveling during convalescence was the most commonly observed major complication; addition of ancillary implants to TPLO significantly reduced its incidence. Postoperative complications were more common in dogs with eTPA than in dogs without eTPA; however, no difference in owner-perceived outcome was identified.
Conclusions— Surgical treatment of dogs with eTPA has a higher complication rate, but comparable outcome to that of dogs without eTPA.
Clinical Relevance— Postoperative TPA≤14° and addition of ancillary implants are recommended when using TPLO to treat dogs with eTPA.